The recognition of atrophic gastritis

Kirkpatrick, J. R.; Davis, Grace; Jacobs, A.; Williams, S W

doi:10.1002/bjs.1800561012

Cited by 3 publications

(2 citation statements)

References 19 publications

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“…Thus, of 12 patients who had multiple biopsies and four patients who had repeat biopsies, only one had more than a 1+ difference in inflammation from one biopsy to aniother, and in only one other was there significant difference in glandular atrophy. Similar findings were reported by Joske et al (1955), Williams et al (1958), Kirkpatrick et al (1969. Exceptions to this are said to occur in antral gastritis and the rare cases of multifocal gastritis.…”

Section: Discussionsupporting

confidence: 87%

Gastric morphology and serum gastrin levels in pernicious anaemia.

Lewin¹,

Dowling²,

Wright³

et al. 1976

Gut

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SUMMARY Mucosal biopsies from multiple sites in the stomachs of 21 patients with pernicious anaemia have been examined. The histological changes almost always involved the entire gastric mucosa, including that of the pyloric antrum. Metaplastic changes were almost universal and consisted of intestinal metaplasia in the body and antrum and pyloric metaplasia in the body. The severity of the pyloric metaplasia was such as to make the distinction between body and antrum on biopsy impossible. No relationship was found between serum gastrin activity and the histological appearances of the gastric antrum or body.The past 25 years have witnessed the introduction of techniques whose application has contributed substantially to the investigation of the nature of chronic gastritis. Peroral suction biopsy (Wood et al., 1949;Joske et al., 1955) of the body and fundus of the stomach has provided a solid histological foundation which, in conjunction with measurements of gastric secretion of acid (Bock et al., 1963) and intrinsic factor and the detection of gastric antibodies (te Velde et al., 1966;Fisher et al., 1967), has considerably extended our knowledge of the pathophysiology of the body of the stomach.In contrast, the structure and function of the gastric antrum was until recently little studied. The introduction of the fibreoptic gastroscope made possible multiple biopsying of the gastric mucosa from well-defined sites in the body and pyloric antrum (Seifert and Knoll, 1968;Konturek and Urban, 1969; Ottenjann et al., 1969a, b) Methods PATIENTSEighteen patients (14 women and four men) referred to our clinic at Stanford University Medical Center with established or suspected PA were studied. Diagnosis was established by failure to secrete detectable acid in response to a maximal dose of gastric stimulant (betazole 1-7 mg/kg body weight) and urinary excretion of less than 10% of a 0-5 Kg oral dose of 57Co B12 in a standard Schilling test, which was corrected with added gastric intrinsic factor. Supporting evidence was low serum vitamin B12 activity, low or absent gastric intrinsic factor secretion, and the presence of circulating gastric antibodies.In addition, studies are included of three patients who were referred for suspected PA but in whom the above criteria were not completely fulfilled (Table 1).

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Section: Discussionsupporting

confidence: 87%

Gastric morphology and serum gastrin levels in pernicious anaemia.

Lewin¹,

Dowling²,

Wright³

et al. 1976

Gut

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“…These diseases were first described in anecdotal reports. Population based surveys were carried out in the 1960s and 1970s [1][2][3][4] and it was demonstrated that NACG can progress to ACG. These studies also showed an association between ACG and the pathogenesis of gastric cancer and other gastric diseases.…”

mentioning

confidence: 99%

Risk factors for atrophic chronic gastritis in a European population: results of the Eurohepygast study

Broutet¹,

Mégraud²,

O’Moráin³

et al. 2002

Gut

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Background and aims: The development of atrophic chronic gastritis (ACG) is multifactorial, involving environment as well as host responses to Helicobacter pylori infection. The aim of this study was to determine factors involved in ACG in a European dyspeptic population. Methods: Data concerning sociodemographics, social behaviour, biological aspects, diet, and virulence factors of H pylori strains were collected in a cross sectional study from 19 European centres in 14 countries. Dyspeptic H pylori positive patients with ACG or non-ACG (NACG) at histology were included. Anti-CagA antibodies were evaluated by two immunoblot tests and anti-VacA antibodies by one. Logistic regression models were constructed, and estimated odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated from the coefficients. Results: Of the 451 patients included in the study, 267 were analysed: 202 had NACG and 65 ACG. Mean age was 44.4 years and 63% were women. Risk factors for atrophy identified by multivariate analysis were: age over 60 years (OR 4.14, 95% CI 1.79-9.58), coffee consumption (OR 2.35, 95% CI 1.07-5.16), sedative consumption (OR 2.17, 95% CI 1.04-4.52), and harbouring anti-CagA and anti-VacA antibodies simultaneously (OR 3.09, 95% CI 1.26-7.56), while the odds were significantly reduced for those with an anxiety score of 6 or more (OR 0.45,. Conclusion:The simultaneous presence of anti-CagA and anti-VacA antibodies enhanced the risk of ACG in European dyspeptic patients. Failure to discern diet and family history as risk factors for ACG may suggest that diet is homogeneous in Europe and that most of the risk factors for ACG identified so far are identical to risk factors for H pylori infection.

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